Case ReportPreeclampsia, HELLP Syndrome, and Postpartum RenalFailure with Thin Basement Membrane Nephropathy: CaseReport and a Brief Review of Postpartum Renal Failure

K. C. Janga , Pavani Chitamanni, Shraddha Raghavan, Kamlesh Kumar,Sheldon Greenberg, and Kundan Jana

Maimonides Medical Center, Brooklyn, NY 11219, USA

Correspondence should be addressed to K. C. Janga; kjanga@maimonidesmed.org

Received 17 February 2020; Revised 16 October 2020; Accepted 28 October 2020; Published 11 November 2020

Academic Editor: Irene Hoesli

Copyright © 2020 K. C. Janga et al. This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

A 36-year-old primigravida female from a birthing center was referred for elevated blood pressure to the hospital two days afternormal spontaneous vaginal delivery with nausea, vomiting, and diarrhea. During this two-day period, she was experiencingpersistent vaginal bleeding and lower abdominal pains for which she took six doses of 600mg ibuprofen. Further laboratoryevaluation reflected leukocytosis, anemia, thrombocytopenia, elevation of liver enzymes, and renal failure with hyperkalemiarequiring emergent hemodialysis once in the Medical Intensive Care Unit (MICU). She was diagnosed with HELLP syndromewith underlying preeclampsia. A week later, due to hypertension controlled with medications and nonoliguric renal failure withno active urine sediments, a renal biopsy was indicated to direct management. The renal biopsy supported the diagnosis ofdiffuse severe acute tubulointerstitial nephritis with hypereosinophilia and thin basement membrane nephropathy (see figures).She was subsequently treated with high-dose steroids which resulted in the normalization of blood pressures and renal functionreturning to baseline. We report the first case of acute tubulointerstitial nephritis in an individual with thin basement membranenephropathy secondary to postpartum complications.

1. Case Summary

1.1. History of Presenting Illness. Our patient is a 36-year-oldfemale primigravida who presented with two-day history ofpersistent postpartum vaginal bleeding, pelvic pain, nausea,vomiting, diarrhea, and poor oral fluid intake. Patient hadreceived prenatal care limited to vitamins and geneticcounselling and went into labor at 41-week-and-4-day gesta-tion at a midwife-assisted birthing center. Castor oil, herbaltea techniques, acupuncture, and various massage maneuverswere used to induce and aid the progression of labor. Thepatient delivered 11 hours after an artificial rupture of mem-branes performed by the midwife. Due to a second-degreevaginal tear and postpartum hemorrhage of unknown etiol-ogy and duration, oral misoprostol and intramuscular oxyto-cin were administered, and the patient returned home. Overthe next day, she had poor oral intake, pelvic pain, and lowurine output. Due to continuing weakness, difficulty walking,

and high blood pressure, she was referred to our medicalfacility. The patient’s past medical history includes easybruising, nosebleeds, and bleeding gums since childhood.Additionally, she used combined hormonal contraceptivesfor three years prior to her current gestation.

1.2. Hospital Course. In the MICU, the patient was in severerenal failure with metabolic acidosis; azotemia; persistenthyperkalemia even after administration of calcium gluconate,insulin dextrose, bicarbonate pushes, and 2 doses of Kayexa-late; hyponatremia unresponsive to fluids; and hypoglycemia.Laboratory findings also included elevated liver enzymes,anemia, thrombocytopenia, leukocytosis, hyperuricemia,subnephrotic-range proteinuria with a urine protein to creat-inine ratio of 0.77 (770mg/dl) and high LDH levels sugges-tive of HELLP syndrome with preeclampsia. The patientwas subsequently started on a nicardipine drip for elevatedblood pressures. Although presenting with no neurologic

HindawiCase Reports in Obstetrics and GynecologyVolume 2020, Article ID 3198728, 7 pageshttps://doi.org/10.1155/2020/3198728

signs, she was started on seizure prophylaxis for eclampsiawith levetiracetam. The patient was also placed on broad-spectrum antibiotics for possible intra-abdominal infection.Though the patient was afebrile, her abdominal pain with leu-kocytosis and history of postpartum hemorrhage promptedinitiation of prophylactic treatment for puerperal sepsis.Differential diagnoses at that time included preeclampsia/-HELLP syndrome, acute fatty liver of pregnancy (AFLP),hemolytic uremic syndrome (HUS), thrombotic thrombocy-topenic purpura (TTP), and puerperal sepsis.

Due to persistently elevated creatinine and refractoryhyperkalemia of 6.3mg/dl not responding to medical ther-apy, the patient underwent one cycle of emergent hemodial-ysis in the Medical Intensive Care Unit. Though her liverfunction tests, platelets, hematocrit, and electrolytes beganto slowly normalize over the next two days, her creatinineremained elevated. She was diagnosed with nonoliguric renalfailure of uncertain etiology requiring a kidney biopsy.

By hospital day 5, the patient’s electrolytes, leukocytosis,thrombocytopenia, and hemolysis parameters normalized(Table 1). Seizure and antibiotic prophylaxes were discon-tinued at that time. Her blood pressure remained elevated,and the patient was deescalated to oral labetalol and amlo-dipine. ADAMTS13 activity levels, ordered on admission,showed a low value of 36.8% (normal 66.8%). However,TTP was ruled out as ADAMTS13 levels should be under10% for this diagnosis. Rare schistocytes were seen on dailyperipheral blood smears; thus, the patient still partially metcriteria for atypical HUS. Immunologic workup and viralpanels for hepatitis and HIV were unremarkable, with theexception of Epstein-Barr virus immunoglobulin titers evi-dent for chronic infection.

On hospital day 6, the patient regained normal appe-tite and she was participating in breastfeeding and out-of-bed exercises conducted in the medical ward. Renalbiopsy results demonstrated acute tubulointerstitial nephri-tis with eosinophils and thin glomerular basement mem-brane (Figures 1–3). Thus, the patient was started on high-dose steroids with a rapid taper over 2 weeks. The manage-ment we provided resulted in normalization of renal function.

2. Renal Biopsy Results

3. Discussion

The syndrome of postpartum renal failure has been recog-nized since 1968 as an idiopathic condition characterizedby renal failure in association with microangiopathichemolytic anemia and thrombocytopenia occurring withina week of apparently normal delivery [1, 2] Postpartumrenal failure is associated with high mortality and morbid-ity primarily from bleeding diathesis and renal failure.Beyond supportive care and hemodialysis, there is no con-clusive evidence that specific therapy is effective in mitigat-ing the hemolytic abnormality or reducing the severity ofrenal failure. Postpartum renal failure can be categorizedbased on etiologies similar to the nonpregnant population(Table 2).

4. Thin Basement Membrane Nephropathyand Pregnancy

Thin basement membrane nephropathy (TBMN) is charac-terized by persistent hematuria and thinning of glomerularbasement membrane. This disease is clinically defined as iso-lated glomerular hematuria, minimal proteinuria, normalrenal function, and a first-degree relative with hematuria. Itis histologically defined by uniform basement membranethinning (on electron microscopic examination) in theabsence of glomerular or interstitial abnormality (on lightmicroscopic or immunological examination). Additionally,WHO criteria for defining TBMN is a basement membranedimension between 250 and 264nm [3]. Causes of TBMNinclude focal segmental glomerulosclerosis (FSGS) and IgAglomerulosclerosis; however, many patients have incidentalbiopsy findings as with our patient.

Clinical complications of TBMN include hematuria,hypertension, proteinuria, and renal failure [4]. Out of these,hypertension and hematuria are the most common compli-cations. However, hypertension in TBMN is not known tobe causal or coincidental. Renal failure is a rare complicationof TBMN and is usually known to be precipitated when asso-ciated with proteinuria, hypertension, and a coexistent tubu-lointerstitial or glomerular lesion as seen in our patient [5].Renal impairment in TBMN is explained by progression ofthe disease itself or more commonly, predisposition to glo-merular or tubulointerstitial lesion [6, 7]. In a study of 16biopsy-proven TBMN patients with acute renal failure, 15of them had coexisting glomerular or tubulointerstitiallesions suggesting the prominent role they play in leadingto renal failure [5]. Whereas lesions like acute tubulointersti-tial nephritis, as seen in our patient, are more likely to becoincidental, lesions like IgA glomerulonephritis needfurther investigation to understand their association.

Although the disease affects >1% of the population, theeffects of TBMN have not been extensively studied in preg-nancy. In a study from 2005, records of parous women witha diagnosis of TBMN over 13 years were reviewed. Majorityof the patients (89.6%) had no complications with an overallfetal outcome of 95% live births and 4.4% fetal loss in <12weeks. Particularly, 3 percent of them developed renal impair-ment, 48 percent developed hypertension, and 53 percentdeveloped proteinuria. Renal impairment was reversible in100 percent of cases [3].

Our patient presented with nonoliguric acute renal fail-ure with hyperkalemia postpartum warranting a session ofemergent hemodialysis. Renal biopsy showed ultrastructuraldiffuse glomerular basement membrane thinning (mean215.06 nm; range 135-287 nm) consistent with thin glomeru-lar basement membrane nephropathy. Although patientswith thin basement membrane nephropathy are known tohave an overall benign course, patients developing protein-uria or hypertension tend to have a higher risk of renal failure[8]. Proteinuria and hypertension in our patient were alsoassociated with elevated liver enzymes and thrombocytope-nia suggestive of a broad differential including preeclampsia,HELLP syndrome, acute fatty liver of pregnancy, and atypicalhemolytic uremic syndrome.

2 Case Reports in Obstetrics and Gynecology

In addition, biopsy finding of acute tubulointerstitialnephritis with hypereosinophilia also suggested acute inter-stitial nephritis (AIN). Overall, the etiology of acute intersti-tial nephritis can be grouped into five general categories:drug-induced, infectious, autoimmune, malignant, and idio-pathic. Out of these, drug-induced AIN accounts for overtwo-thirds of all cases and, although many drugs have beenimplicated, nonsteroidal anti-inflammatory drugs (NSAIDs)and antimicrobial agents have been seen to cause the major-ity of these cases. It is understood that the pathogenesis ofAIN is an immunologic reaction via endogenous nephrito-

genic or exogenous antigens that are presented by tubularcells to T cells, activating a cascade of effector cells and cyto-kines eventually leading to interstitial infiltrates [9]. Eitherpatchy or diffuse infiltrates of lymphocytes, macrophages,and plasma cells are commonly seen on renal biopsy, suchas in our patient, along with nonsuppurative fluid withinthe interstitium and/or tubules. The laboratory findings,showing impairment in kidney function, can vary from selec-tive abnormalities of tubular function to acute renal failurewith or without oliguria. Historically, BUN and creatininewill increase after tubular dysfunction is detectable, with orwithout oliguria. The presence of a history consistent withAIN and laboratory findings of acute kidney injury are suffi-cient to diagnose this condition, although definitive diagnosisis through renal biopsy. Reversal of kidney injury is the rulein 60-65% of cases after the removal of offending agents.The use of steroids in AIN remains controversial but deservesconsideration, as it has been shown to have better outcomesfor patients when started early in the disease course [9, 10].The etiology of AIN in our patient was likely the recent useof NSAIDs prior to delivery.

5. Differential Diagnoses

At presentation, the patient met the criteria for preeclampsiawith hypertension, proteinuria with urine protein to creati-nine ratio of 0.77, elevated creatinine and transaminases,and thrombocytopenia suggestive of end-organ damage(Table 3). Currently, preeclampsia is one of the most preva-lent medical complications of acute kidney injury in womenand the most reported complication in those women requir-ing dialysis in the postpartum period [11].

Table 1: Laboratory values of the patient over the course of her hospitalization.

Day 1 Day 3 Day 5 Day 7 Discharge 3-week follow-up

Glucose 40 147 73 109 96 83

Hemoglobin 8.9 8.5 7.9 7.4 7.0 11.4

WBC count 23.7 16.6 9.1 8.0 8.6 6.4

Eosinophils (%) 0.0 0.0 1.1 1.6 0.0

Platelet count 57000 115000 144000 183000 253000 211000

Creatinine 5.3 4.7 5.6 5.3 2.1 1.0

BUN 57 45 61 66 53 17

AST 650 166 45 32 18 13

ALT 1308 708 313 184 91 15

ALP 143 142 119 111 102 69

Sodium 113 126 123 132 142 140

Potassium 6.6 4.4 4.2 4.6 4.8 4.0

Bicarbonate 17 20 19 19 21 30

Bilirubin 0.8 0.5 0.4 0.4 0.4 0.4

PT 10.2 11.2 11

PTT 26.5 30.3

INR 0.9 0.9 0.9

LDH 448 360 278 224

WBC: white blood cell; BUN: blood urea nitrogen; AST: aspartate transaminase; ALT: alanine transaminase; ALP: alkaline phosphatase; PT: prothrombin time;PTT: activated partial thromboplastin time; INR: international normalized ratio; LDH: lactate dehydrogenase.

Eosinophils

Interstitial edema

Figure 1: Light microscopy findings indicative of diffuse severeacute tubulointerstitial nephritis with eosinophils.

3Case Reports in Obstetrics and Gynecology

The pathogenesis of preeclampsia occurs in several ways.It involves defects in placentation mediated by placental-derived angiogenic factors, such as placental growth factoror soluble endoglin. Along with dysfunction of the comple-ment system, errors in placentation can cause severe kidneyinjury. Without maternal susceptibility, the complementsystem is activated in normal pregnancy. However, it is exag-gerated in preeclampsia and studies have found this exacer-bation cytotoxic to cells [12]. It has also been found thatpreeclampsia has a direct effect via endothelial injury, vaso-constriction, inflammation, and the overactivation of thecoagulation cascade. These mechanisms are sufficient enoughto cause catastrophic organ complications and are responsiblefor high admission rates to the intensive care unit.

HELLP syndrome was also part of the differential asthe patient had evidence of hemolysis with elevated liver

enzymes and low platelet count (Table 4). This syndromecan present up to 7-day postpartum and is a milder form ofmicroangiopathic hemolytic anemia due to a dysregulationof the complement pathway. Postpartum complicationsinvolve bleeding requiring transfusions, DIC, pulmonaryedema, and renal failure in 10% of recorded cases. Manage-ment is usually supported including magnesium sulfate, anti-hypertensive medications, and blood transfusions forHb < 7,and platelet transfusions for <30K. This syndrome is self-limiting in the postpartum phase, and trending the plateletcounts is used as a prognostic indicator [13, 14].

Though acute fatty liver of pregnancy (AFLP) is knownto typically present between the 30th and 38th week of preg-nancy, few cases have been reported to occur postpartum[15]. General clinical symptoms that can be present at thetime of diagnosis are nausea, vomiting, abdominal pain,

Peritubular fibrin

Tubule

Tubule

(a)

Peritubular capillarylumens

(b)

Figure 2: (a, b) Light microscopy shows fibrinoid necrosis of the peritubular areas suggestive of microangiopathy.

74 nm

287 nm

1677 nm90.6 nm

154 nm

184 nm

(a)

234 nm

187 nm

244 nm172 nm

184 nm

227 nm

240 nm

(b)

Figure 3: (a, b) Electron microscopy demonstrates diffuse glomerular basement thinning with arithmetic mean 215.06 nm (range 135-287 nmwith 100% of 41 measures less than 300 nm and 63% less than 215 nm).

4 Case Reports in Obstetrics and Gynecology

and jaundice. The pathogenesis of this disease involvesmaternal and fetal mutations in the enzyme long-chain 3-hydroxyacyl-CoA dehydrogenase, which processes long-chain fatty acids (LCFA). With dysfunction of this enzyme,LCFAs accumulate and cause hepatotoxicity. Thus, althoughbiopsy is not usually performed, it would demonstrate micro-vesicular fatty infiltration of hepatocytes [12]. Pregnancy-related acute kidney injury is present in over half the casesof AFLP, as these LCFAs can deposit in the renal tubular epi-thelium. Our patient similarly reported nausea and vomitingin the postpartum period. A large degree of clinical overlap isvery often seen between AFLP, HELLP, and preeclampsia[16]. With elevated transaminases, hypoglycemia, lactic aci-dosis, and thrombocytopenia, she fell into the spectrum ofthis disease, although her hypertension also placed her diag-nosis in the realm of preeclampsia/HELLP syndrome. Sincedistinguishing between AFLP and preeclampsia/HELLP can

Table 2: Causes of renal failure in pregnant and nonpregnant patients.

Etiologies of renal failure Conditions related to pregnancy Conditions unrelated to pregnancy

Prerenal

Hyperemesis gravidarum, vomiting due topreeclampsia, HELLP/AFLP, hemorrhage(missed abortion, septic abortion, placental

abruption, placenta previa, uterine previa, bleedingduring surgery, uterine laceration, uterine perforation)

Vomiting due to infections, gastroenteritis,pyelonephritis, malnutritionOthers (like diuretics, CHF)

Intrinsic renal

ATN/ACN: preeclampsia, HELLP, AFLP, amnioticfluid embolism, pulmonary embolism

TMA: HUS, preeclampsia, HELLP, AFLP, DIC,underlying glomerular diseases

ATN, de novo glomerular disease, AIN

PostrenalBilateral hydronephrosis

Trauma to the ureters and bladder during surgery

Bilateral ureteral obstruction stone/tumorTubular obstruction (meds/calcium/uric acid)

Obstruction at bladder outlet

Renal allograft related Similar to nonpregnant conditions

Acute rejectionATN

Acute interstitial nephritis,calcineurin inhibitor toxicity,CMV/BK virus nephropathy,

postinfectious glomerulonephropathy

HELLP: hemolysis, elevated liver enzymes, low platelet count; AFLP: acute fatty liver of pregnancy; CHF: congestive heart failure; ATN: acute tubular necrosis;ACN: acute cortical necrosis; AIN: acute interstitial nephritis; TMA: thrombotic microangiopathies; HUS: hemolytic uremic syndrome; DIC: disseminatedintravascular coagulation; CMV: cytomegalovirus.

Table 3: Diagnostic criteria for preeclampsia fulfilled by our patient.

Preeclampsia criteria Our patient’s laboratory results on admission Met or unmet

Blood pressureNew-onset hypertension after 20 weeks of

gestation (>140/>90 on 2 occasions at least 4 hapart or >160/>110 within short minutes)

Postpartum blood pressure of 140/60mmHg,with continuous elevated readings

during hospitalizationMet

ProteinuriaHypertension plus >300mg/24 h urine collection,protein/creatinine ratio of >0.3, or urine dipstick

reading of 1+Protein/creatinine ratio of 0.7 Met

End-organ damage

Blood pressure criteria plus evidence ofthrombocytopenia (platelet < 100K), renalinsufficiency (creatinine > 1:1 or doubling),impaired liver function (transaminases twicethe normal), pulmonary edema, cerebral or

visual symptoms

Platelets: 68,000/μl

Met

Creatinine: 5.3mg/dl

AST/ALT: 650/1308

AST: aspartate transaminase; ALT: alanine transaminase.

Table 4: Diagnostic criteria for HELLP syndrome fulfilled by ourpatient.

Definition Laboratory rangeMet orunmet

Hemolysis

Peripheral smear: schistocytesand burr cells (>5/HPF)

Yes

Serum bilirubin: >1.2mg/dl No

Haptoglobin: <25mg/dl Yes

LDH > 2x the upper limit of normal Yes

Anemia: Hgb < 7 and not relatedto blood loss

Yes

Elevated liverfunction tests

AST/ALT > 2x the upper limit of normal Yes

Low platelets <100,000 cells/μl Yes

AST: aspartate transaminase; ALT: alanine transaminase.

5Case Reports in Obstetrics and Gynecology

be difficult due to similar parameters of disease, manypatients, about 20-40% with AFLP, have a simultaneousdiagnosis of preeclampsia/HELLP [12].

Thrombotic microangiopathies were also considered animportant differential as the patient had hemolytic anemia,acute kidney injury (AKI), and thrombocytopenia. However,thrombotic thrombocytopenic purpura was ruled out asADAMTS13 levels were >10%. Atypical hemolytic uremicsyndrome (HUS) was still a possibility with marked effecton renal function requiring renal replacement therapy. Inthe postpartum period, loss of placental protective barriermechanisms, inflammation, infection, wounded uterus, andinflux on fetal cells can trigger systemic activation of alterna-tive complement cascade. Genetic mutations in the regula-tory proteins (factor-H, I, CD-46) or complement activators(C3, factor-B) of the alternative complement pathway arefound in 50% of the cases [13, 17, 18].

Preeclampsia, AFLP, and HELLP syndrome are com-monly associated with cortical or acute tubular necrosis onrenal biopsy [19] whereas atypical HUS shows fibrinoidnecrosis of arterioles and thrombus in the lumen extendingto the glomerular capillary tufts [18]. However, renal biopsyin our patient showed acute tubulointerstitial nephritis withhypereosinophilia and thinning of the basement membranesuggestive of acute interstitial nephritis with thin basementmembrane nephropathy. A rare focus of microscopic peri-tubular fibrin and necrosis was also present (Figure 2(a)) sug-gestive of a microangiopathy; however, other features ofthrombotic microangiopathy (e.g., arterial, arteriolar, or glo-merular angiopathy/ultrastructural endotheliosis) were notidentified.

In conclusion, we present a case of renal failure in thepostpartum period in which an array of factors were consid-ered. Predisposing risk factors for postpartum renal failureinclude nephrotoxic medications, infections, proteinuria,cystic diseases, chronic kidney disease, transplant, and glo-merular diseases. As outlined by our review article, a few ofthese causes include medication use like NSAIDS in the peri-partum period and gestational disease including preeclamp-sia and HELLP syndrome, as well puerperal sepsis in thepostpartum obstetrical infections. Our patient was success-fully treated with prompt supportive therapy and a shortcourse of high-dose steroids with normalization of renalindices and urine proteinuria. In such cases of renal failurespecifically in the postpartum period, the etiologies contrib-uting are overlapping each other leading to a complex pre-sentation which requires a multidisciplinary approach inthe treatment geared towards addressing each of the specificcauses [20].

Data Availability

All data generated or analyzed during this study are includedin this published article.

Conflicts of Interest

The authors declare that they have no conflicts of interest.

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7Case Reports in Obstetrics and Gynecology